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Titolo:
Microglial interaction with beta-amyloid: Implications for the pathogenesis of Alzheimer's disease
Autore:
Bamberger, ME; Landreth, GE;
Indirizzi:
Case Western Reserve Univ, Sch Med, Alzheimers Res Lab, Dept Neurosci, Cleveland, OH 44106 USA Case Western Reserve Univ Cleveland OH USA 44106 Cleveland, OH 44106 USA
Titolo Testata:
MICROSCOPY RESEARCH AND TECHNIQUE
fascicolo: 2, volume: 54, anno: 2001,
pagine: 59 - 70
SICI:
1059-910X(20010715)54:2<59:MIWBIF>2.0.ZU;2-M
Fonte:
ISI
Lingua:
ENG
Soggetto:
TUMOR-NECROSIS-FACTOR; INTEGRIN-ASSOCIATED PROTEIN; NITRIC-OXIDE SYNTHASE; NONSTEROIDAL ANTIINFLAMMATORY DRUGS; MACROPHAGE SCAVENGER RECEPTOR; SIGNAL-TRANSDUCTION PATHWAYS; LOW-DENSITY LIPOPROTEINS; CENTRAL-NERVOUS-SYSTEM; NEURONAL PC12 CELLS; PPAR-GAMMA AGONISTS;
Keywords:
inflammation; beta-amyloid; receptors; neurotoxicity; signal transduction; NSAIDs; microglia; Alzheimer's Disease;
Tipo documento:
Review
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
143
Recensione:
Indirizzi per estratti:
Indirizzo: Landreth, GE Case Western Reserve Univ, Sch Med, Alzheimers Res Lab, Dept Neurosci, E504,10900 Euclid Ave, Cleveland, OH 44106 USA Case Western Reserve Univ E504,10900 Euclid Ave Cleveland OH USA 44106
Citazione:
M.E. Bamberger e G.E. Landreth, "Microglial interaction with beta-amyloid: Implications for the pathogenesis of Alzheimer's disease", MICROSC RES, 54(2), 2001, pp. 59-70

Abstract

The etiology of Alzheimer's disease (AD) involves a significant inflammatory component as evidenced by the presence of elevated levels of a diverse range of proinflammatory molecules in the AD brain. These inflammatory molecules are produced principally by activated microglia, which are found to beclustered within and adjacent to the senile plaque. Moreover, long-term treatment of patients with non-steroidal anti-inflammatory drugs has been shown to reduce risk and incidence of AD and delay disease progression. The microglia respond to beta-amyloid (AP) deposition in the brain through the interaction of fibrillar forms of amyloid with cell surface receptors, leading to the activation of intracellular signal transduction cascades. The activation of multiple independent signaling path ways ultimately leads to the induction of proinflammatory gene expression and production of reactive oxygen and nitrogen species. These microglial inflammatory products act in concert to produce neuronal toxicity and death. Therapeutic approaches focusedon inhibition of the microglial-mediated local inflammatory response in the AD brain offer new opportunities to intervene in the disease. (C) 2001 Wiley-Liss, Inc.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 29/09/20 alle ore 10:04:03